Developmental Toxins, Carcinogens, and Mutagens and their Concentrated Presence in Breast Milk


Note:  Much of the information in this section is somewhat technical, and it is rather lengthy.  As an introduction to it, we will begin with a brief presentation of some specific points about why people should be re-examining their positions on breastfeeding, and will then touch briefly on information about infant exposures to toxins as well as apparent effects of the toxins of concern.



The U.S. Surgeon General acknowledges that "research on the health outcomes of different modes of infant feeding is limited to observational studies, the results of which can only provide inferences...."1   Because of "confounders" (underlying, actual causes of the associations found in studies), the U.S. Agency for Healthcare Research and Quality points out that observational studies are subject to "false conclusion."2



Norway is at the very top level of the world's long-standing high-breastfeeding countries.3  There is therefore extra credibility in a statement about effects of breastfeeding if it is made by researchers from the Norwegian University of Science and Technology, especially when they are summarizing "the largest study that has been done on breastfeeding and health."  That study was apparently also the only breastfeeding study that has utilized randomization, the best way to avoid effects of confounders.  Their statement was as follows:  "This study cuts the legs out from underneath most of the assertions that breastfeeding has health benefits." 4



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Many scientific studies have found that health outcomes are worse among children who were more breastfed than among children who were breastfed less or not at all, with at least 26 such studies in the categories of asthma, allergies and diabetes alone, three regarding autism, and one finding a dose-response relationship between toxins in breast milk and behavior scores in the breastfed children indicating likelihood of later having ADHD.5



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Average daily exposure of a breastfed infant to dioxin toxicity over the period of a year, as estimated by the EPA, is over 80 times higher than the reasonably-safe upper threshold of dioxin exposure estimated by the EPA.6



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The Danish scientist who is author of nine studies on chemical contamination of human milk and 40 other studies, as well as Head of the Section of Environmental Technology of the Danish Institute of Technology, said, "The average levels of persistent organohalogens in human milk are normally 10 to 20 times higher than the levels in cow's milk or infant formulas." 7   Organohalogens include dioxins, PCBs and PBDEs, all of which are neuro-developmental toxins; all of them are also part of diesel emissions.8  Note that diesel emissions were one of only two pollutants that were most strongly implicated in the 2013 Harvard study that found close correlations between autism diagnoses and environmental pollution at the times and places of the children's births.9



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A  U.S. study of all 50 U.S. states and 51 U.S. counties, carried out by a highly published scientist and Fellow of the American College of Nutrition, found that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."10  


Two other studies, in the U.S. and U.K., came to conclusions similar to the above, with a dose-response relationship between breastfeeding and autism indicated by comparing the findings of the two studies.11



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"Overwhelming evidence" (as stated by the UCLA Food & Drug Allergy Care Center) suggests that "the hygiene hypothesis explains most of the allergy epidemic."12  According to that, there are too few microbial challenges in our current environments in developed countries to properly stimulate development of the immune system.  So the undisputed immune cells in breast milk are further reducing challenges that apparently already have become too low for proper development of children.


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In the decades following the major increase of U.S. breastfeeding rates beginning in the 1970's, not one of the disorders alleged by Surgeon General Regina Benjamin to be reduced by breastfeeding declined, as indicated by data from the CDC and other authoritative sources.  In fact, all but one actually increased substantially, often in precise correlation with major variations in the breastfeeding rate increases.13


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There is one piece of advice about breastfeeding from earlier decades that still has validity, which is that lactation reduces a woman's body burden of persistent toxins (by means of excreting those toxins in breast milk); and it therefore might reduce her risk of cancer.  But, seeing the extremely close correlations between breastfeeding rates and incidences of childhood cancer14 as well as autism, some mothers are starting to question whether it is desirable to transfer those toxins to their rapidly-developing babies at the most vulnerable times of the infants' lives.


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Criticisms of any of the points above are earnestly requested, if you feel that anything said is not an accurate representation of information from authoritative sources (see sources below).  Our intention is to make this website as accurate as possible.  Please make any comments specific regarding any statements you consider not to be accurate in relation to the sources. Or indicate why any sources indicated are not trustworthy.  Please send any responses to , and they will be posted below.  Thank you for your attention to this important matter.



The compete presentation about toxins in breast milk and formula, and their effects will follow right after this set of footnotes.




Footnotes for introductory section:


(1)  Surgeon General's Call to Action to Support Breastfeeding, 2011, p. 33 at


(2)   Agency for Healthcare Research and Quality, U.S. Dept. of Health and Human Services, Systems to Rate the Strength of Scientific Evidence, Evidence Report/Technology Assessment: Number 47  at


(3)  See, noting Norway's 6-month rate in the Europe chart and then seeing the 6-month breastfeeding rates in the World data set, with only Mongolia and Rwanda sharing the top position.


(4)  "Breastfeeding is not as beneficial as once thought" (06.01.2010) published by the Norwegian University of Science and Technology, at  Their statement was based on findings of the PROBIT study in Belarus. (This article, on the website of the Norwegian University of Science and Technology, indicated no author; it therefore appears to be an established, official statement of the University, dated 2010 and accessed in 2013.)


(5)  See


(6)  Estimating Exposure To Dioxin-Like Compounds - Volume I: U.S. EPA, EPA/600/8-88/005Ca., 2002, revised 2005 –,  Section II.6, "Highly Exposed Populations" (p. 39)  The EPA estimated 60 pg of TEQ/kg-d of exposure.  For comparison, Jensen et al. (see footnote 7, p. 249), estimated between 50 and 100 pg of TEQ/kg-d.  

Also  in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day." (that is, O.7 pg of TEQ/kg-d)   In the EPA’s “Glossary of Health Effects”, RfD is defined:  “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”


(7) Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p. 287. (Many libraries would not have this, but it should be available as an Inter-Library Loan.)


(8) (Dioxins and PCBs are well-known components of diesel emissions, and PBDEs are also present in those emissions): Aerosol and Air Quality Research, 11: 709–715, 2011 Copyright © Taiwan Association for Aerosol Research ISSN: 1680-8584 print / 2071-1409 online doi: 10.4209/aaqr.2011.05.0058 Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters Lien-Te Hsieh et al. at


(9) Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, Roberts et al., published June, 2013 in Environmental Health Perspectives, at .


(10) Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at


(11)  Breastfeeding and Autism  P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot, found at   The percent of ASD-diagnosed patients who had been breastfed at 6 months was 37%, as compared with 13% in the control group (or 14% in the general Kentucky population). Also Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14   Paul Whiteley (Department of Pharmacy, Health & Well-being, Faculty of Applied Sciences, University of Sunderland, UK), et al.  Autism Insights 2009:1 3-17  at    Also:  Patterns of breastfeeding in a UK longitudinal cohort study, Pontin et al., School of Maternal and Child Health, University of West of England, Bristol, UK.    The records showed that 65% of the children with those conditions had been “exclusively breastfed” for over four weeks.  After doing a search of available sources for a comparison figure for exclusive breastfeeding for over four weeks for the U.K. as a whole for the period in which those children would have been newborns, this author has come up with data from two different sources, which are consistent in leading to a figure of about 28%.  This is a lower ratio of cases to general population compared with the Williams study, in a study in which the duration of the breastfeeding being compared was also lower than in the Williams study.


(12)  "About Allergies/ Why Are Allergies Increasing?" found at



(13)  See


(14)  See




And now the details about toxins in breast milk and formula, and their effects:

In the words of the U.S. Agency for Toxic Substances and Disease Registry, with emphasis added:  "The proper development of many systems and functions (in an infant) depends on the timely action of hormones...; therefore, interfering with such actions can lead to... altered metabolic, sexual, immune, and neurobehavioral functionsEffects of this type...occur following exposure....early in life caused by either direct exposure to chemicals or exposure (to environmental chemicals) via maternal milk."(28)  (The text segments that applied directly to the present discussion were selected from the original text; the complete text can be found at the footnote shown.)


How these chemicals cause harm:  One important form of dioxins is a known carcinogen, other forms of dioxins are classified as likely carcinogens, and PAHs are well known to cause cancer in animals.28a   One specific means by which dioxins, BPA and at least one PAH cause neuro-developmental harm is by acting as "endocrine disruptors."   A web page of the National Institutes of Health says that endocrine disruptors are "chemicals that may interfere with the body’s endocrine system and produce adverse developmental, reproductive, neurological, and immune effects in both humans and wildlife. …. ." (emphasis added)   Some PAHs have been identified as mutagens, which can have adverse effects on the ways organs including the brain develop.


Quoting from the NIH's web page on endocrine disruptors, "Endocrine disruptors …may mimic or interfere with the function of hormones in the body. Endocrine disruptors may turn on, shut off, or modify signals that hormones carry,…" (emphasis added) (30)  Continuing, "Research shows that endocrine disruptors may pose the greatest risk during prenatal and early postnatal development when organ and neural systems are developing.   According to the Committee on Developmental Toxicology of the National Academy of Sciences, ”Agents that interact with one or more of these receptors and are known to produce abnormal development include ……dioxin (TCDD)."  Explaining how dioxin affects the developing body, the NAS committee points out that it "... alters the expression of several dozen genes, one or more of which might result in an adverse developmental outcome." (31)  (emphasis added) 


Sources of these toxins:  The EPA's web pages and documents on dioxins and PAHs point out major sources of dioxins and PAHs as follows:  (a) dioxins are unintentional byproducts of several industrial chemical processes and of most forms of combustion, including wildfires, backyard burning, municipal solid waste and industrial and hospital incineration, vehicle exhaust (mainly diesel emissions), and emissions from oil- or coal-fired power plants, and are also found in weed killers and in ordinary soil onto which dioxins have settled and been precipitated out of the atmosphere; (b) PAH's are also unintentional products of typical forms of combustion, including cigarette smoking, residential wood burning and vehicle emissions.(34)  (Note that most of the above sources are related to population density and combustion processes.)  Animal fat in the diet accounts for close to 90% of dioxin exposure in the United States, according to a 2003 National Academies of Science report on dioxins in the food supply. (34a)  Vegetarians are reported to consume only 2 percent of the dioxin load of the general population, because their diet is dominated by foods low on the food chain. (34d)  Most human intake of PBDEs comes from dust released by electronic devices within homes and buildings.  Human exposure to BPAs comes mainly from plastic packaging of food and metal cans.


The predominant source of high doses of these toxins to infants

To provide an idea of how much dioxin is a significant hazard to human infants, note that (in its most recent dioxin assessment, issued February, 2012), the EPA set the threshold for safe dioxin exposure at a toxicity equivalence (TEQ) of 0.7 picograms per kilogram of body weight per day.(34b)  Note that what appears to be the only EPA estimate of infant exposure to dioxins predicts that an infant breastfed for one year would receive an average daily dose of about 60 pg of TEQ/kg bw/day.(34c)   So the average daily dose of 60 pg, over the period of a full year of rapid development, is 86 times the estimated safe dioxin exposure of 0.7 pg. 


The above figures are estimated average daily exposures over a full year of breastfeeding, taking into account the lower levels that occur later in the year during the course of excretion by way of lactation.  The peak body-weight-based dose received by a breastfeeding infant is estimated in an EPA study to be 242 pg TEQ/kg-day.(37a)   Note that these extremely unsafe exposures of breastfed infants come at the most vulnerable times of their lives for neurological development, and they come shortly before a high-level period for development of childhood cancer. (see



Concentration of toxins in breast milk, causing many-times higher infant intake than from formula or from trans-placental exposure:

According to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR), ”PCBs tend to accumulate in breast milk fat,” with accumulations increasing with the woman’s age. (82a)  A study cited by the ATSDR showed the intensity of concentration of PCBs in breast milk:  “Daily PCB intake for native northern Quebec women was calculated to be 0.3 μg/kg (ppb) body weight while daily intake among infants was calculated to be 10 μg/kg due to breast feeding. (Section 6, p. 584)  That means that, at least as found in this study, toxins that enter the woman’s body are excreted in breast milk in what is effectively a 30-times-higher concentration compared with their entering concentration.  A study in the Netherlands, also summarized by the ATSDR (p. 569), found that, at 42 months of age, the median plasma PCB levels of children who had been breastfed for at least 6 weeks were 4½ times as high as those of children who had been formula-fed.

The above two comparisons implied the nature of, but didn't specify, the ratio of PCBs taken in by a breastfed infant compared with the intake of an adult.  A figure for that is provided by a commission of the German Federal Environmental Office, which reported that the average daily intake of an adult is 0.02 micrograms of PCBs per kg of body weight, as compared with the intake of a breastfed infant, which is 3 micrograms per kg of body weight, or 150 times higher.(82c)  

It might seem that growing for nine months inside a mother's body would put a fetus at maximum vulnerability for exposure to toxins that have accumulated in the mother, but apparently that exposure can be minor compared with the effects of breastfeeding.  According to what is apparently the most thorough study on the subject of infant absorption of toxins from mother's milk vs. from fetal absorption, "Significantly more (10 to 20 times) of a mother's body burden of persistent organohalogens is transferred to the infant via the milk than by the transplacental route." (Note that dioxins, PCBs and PBDEs are included among organohalogen compounds.)  Tests with animals have confirmed the above, with even higher ratios of lactational vs. transplacental transfer. (81b) 


According to an EPA report, providing estimates for typical exposure in the U.S. based on EPA data but also drawing on studies of populations in Germany (two studies), Britain and the Netherlands, "Breast-feeding for 6 months or more is predicted to result in an accumulated (dioxin) exposure 6 times higher than a formula-fed infant during the infant's first year of life.”. (83)   A German study found that intake of dioxins was up to 50 times higher in breast-fed infants compared with formula-fed, and also that high proportions of the dioxins were intestinally absorbed by the breastfed infants.  At 11 months of age, the dioxin toxicity-equivalent concentrations in the formula-fed infants were about 10 times lower than in the infants that were breast-fed for six to seven months. (85)   This study (Abraham et al.) was cited in a 2002 EPA document ("Infant Exposure to Dioxin-like Compounds in Breast Milk") that apparently considered it to be fully valid. (37a)  

However, the 6- or 10-times-higher range of long-term accumulation or concentration in the breastfed infants may understate the reality of the harm caused, since the "up to 50 times higher" short-term exposure may result in unusual harm just during that short-term period; this is especially likely to be the case since higher doses come earlier in the lactational period, when the "window of sensitivity" for neurological development is likely to be taking place (see Section 1.2.b.1 at

The presence of these "persistent" toxins in the child's body declines after their rapid buildup during breastfeeding, but only very gradually.   PCB levels in children who had been breastfed for at least 12 weeks were still over twice as high as in bottle-fed children at 7 years of age, in an American/German study. (82b)


The EPA's 2010 Exposure Assessment of PBDEs found an estimated total adult intake dose of 7.1 ng/kg-day (nanograms per kilogram of body weight per day).   Comparing with various figures for other age groups, "infant intakes due to ingestion of mother’s milk were the highest at 141 ng/kg/day."  So the average effective intake of a breastfeeding infant from mother's milk alone is 20 times the average total intake of adults.  On top of that, infants also take in far more PBDEs than adults do from dust, and dust is by far the largest source of PBDE exposure to the general population. (81c)  In the only comparison the EPA provides of PBDE food intake by a breastfed infant compared with food intake of PBDEs by an average adult, the breastfed infant was estimated to take in over 200 times as much as the adult.(81d)  See farther down about developmentally-toxic effects of PBDEs (apparently leading to greatly increased likelihood of ADHD) and their extremely rapid increases in the environments of developed countries in recent decades.

PBDEs in breastfed vs. bottle-fed children:  In the only study quoted by the EPA making such a comparison, based on measurements of 244 children (Carrizo et al., 2007), the average total concentration in children that had been breast fed was still nearly three times as high as average concentrations in formula-fed children at age 4 (3.6 vs.1.3 ng/g lwt).(81e)  This is as should be expected, judging by the differences in PBDE concentrations found in infant formula vs. breast milk, as follows:  In the only data regarding PBDE concentrations in infant formula that is provided in the EPA's PBDE Exposure Assessment (citing Schechter et al., 2006 a), two samples of infant formula were found to have PBDE concentrations of 32 and 25 pg/g wwt (wet weight), respectively. (81f)  Going by EPA data, total PBDE concentrations in mother's milk average about 1760 pg/g wwt or higher.(81g)  Such a difference in contents of this toxin between human milk and formula is not surprising, considering that about 90% of human intake of PBDEs comes from dust released by electronic devices within homes and buildings, according to the EPA; cows and soybean plants (the chief sources of alternatives to breast milk) obviously don't live inside houses containing TVs, computers and other electronics.


Mercury (another of the "persistent, bio-accumulative toxins" that increase greatly with each step up the food chain) would clearly accumulate more in humans who eat fish, especially large fish, than in cows.  (The EPA says that "Nearly all methylmercury exposures in the U.S. occur through eating fish and shellfish."(81y)) In a 2013 Harvard University study, five environmental pollutants at time and place of birth were found to be specifically connected with likelihood of later autism diagnosis of the child; two were especially strongly associated with autism; mercury was one of those two.(81w)  That study's research drew on a far larger base of data than any previous study on the subject.  


According to EPA-contracted researchers, "A wealth of information on the pharmacokinetics of Hg and MeHg (mercury and a mercury compound) exists in the available literature (extensively reviewed by U.S. EPA, 1997b). Together, the data indicate that the lactational transfer of Hg during the first 15 days of lactation accounts for roughly one-third of the transfer of Hg during gestation."(81t)  Notice that, in just 15 days of breastfeeding, an amount of mercury is transferred to the infant equal to one third of the entire amount that was transferred during the many months of gestation.  The placenta provides some shielding of the fetus from toxins; and ingestion in food is typically an efficient means of absorption of toxins.  Judging by the above quotation, it seems probable that total transfer of mercury during lactation would typically be greater than the mercury transferred during gestation.


In addition, retention of the transferred mercury is apparently greatly increased by infant consumption of milk or formula as opposed to solid food.  A study of mercury retention by infant monkeys found that both blood and hair mercury showed a sudden drop directly after weaning, which was accompanied by a several-fold increase in fecal mercury excretion." (81v) (See chart below.)


The mechanism that causes this to take place (retention of mercury during breastfeeding, stopping after weaning) seemed to be unknown (milk facilitating gut absorption of ingested mercury, or solid food promoting flow of intestinal content containing or binding to mercury?).  But it appears to be clear that milk-feeding vs. solid-food feeding makes the difference between major buildup (or continued buildup) of mercury in the infant's body and excretion of most of the mercury.


Note that monkeys, like humans, are primates.  Since humans aren't used as laboratory animals, what happens in monkeys' bodies probably provides the closest available approximation of what happens inside human bodies.



Notice in this chart that most of the brain's growth and development (especially of the cerebellum) takes place during the first year after birth, while most breastfeeding takes place.   And note that "there is increasing recognition that the cerebellum contributes to cognitive processing and emotional control in addition to its role in motor coordination."(81u)






To sum up some preceding information:

Transfer of mercury to infants by lactation is apparently much faster than during gestation.  And mercury's excretion from the infant's body is apparently greatly retarded by milk-type feeding.  Aside from mercury, 10 to 20 times as much of a mother's body burden of organohalogens (heavily present in diesel emissions) is transferred to the infant in breast milk than is transferred during gestation. (see above)  Remember also from earlier that mercury and diesel emissions are the two environmental pollutants that were identified in a 2013 Harvard study as being most closely linked to incidence of autism. 


Milk is far higher in mercury in lactators who eat fish and have amalgam fillings (i.e., human mothers) than in those that don't (i.e., cows); and organohalogens are many times higher in human milk than in cow's milk or formula (see above). So both of the two specific pollutants that have been most closely implicated with likelihood of autism become greatly increased in the infant by breastfeeding.


Consider the above in relation to the fact that most of the brain's growth and development takes place during the first year after birth (see chart above/right).  


Also consider all of the above in relation to the finding by a highly-published scientist and Fellow of the American College of Nutrition, concluding a U.S. study of all 50 U.S. states and 51 U.S. counties, that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."(81x)



In order to appreciate the fact that typical breast milk in nursing mothers these days is very different from that of earlier times, one should be aware of the following:


1) Estimates from various studies suggest that rates of dioxin deposition in the environment (mostly from the air) increased more than 10-fold between the 1930s and the late 1960s. (86)  Smokestack sources of dioxins have declined recently, but sources in the U.S. that reach populated areas intensively (dioxins in diesel emissions) have continued to greatly increase, as of the most recent data; (96) and those "persistent" toxins continue building up in the environment, especially in soil (and from there back into the air, water and food supply).  Remember from earlier how far dioxin contents of typical breast milk have been found by the EPA to exceed the EPA's estimated safe level, and also bear in mind from just-preceding paragraphs how far a breastfed infant's ingestion of dioxins exceeds that of an infant that has not been breast fed.

2) The average dioxin content per ounce of animal-based foods is much higher than in earlier times, following the increases of toxins in the environment. The U.S. Agency for Toxic Substance and Disease Registry says that "eating food, primarily meat, dairy products, and fish, makes up more than 90% of the intake of CDDs (dioxins) for the general population." (88)  Farm animals and fish ingest and build up persistent toxins in their tissues largely as a result of what they eat, meaning vegetation and sediment onto which the greatly-increased levels of dioxins and mercury from the environment have been deposited; in addition there is "bio-magnification" as the increasing accumulated concentrations of toxins in animal tissues and dairy products (especially in the fat content) are passed up the food chain (via smaller fish being eaten by larger fish, and animal-based products being eaten by humans).

3) "Meat consumption has more than doubled in the United States in the last 50 years," (89)  while the population only increased 72%.  

Heavy metals:

Other neurological toxins or carcinogens of concern are contained within breast milk.  Quoting from page 12 of an IFCS FSC Working Group paper, "Heavy metals such as methylmercury and lead are also secreted in breast milk."   According to the EPA, mercury in the ­atmosphere tripled between the era before human activity and current times,(254) and it continues to increase moderately rapidly, coming from many combustion sources (especially coal-fired power plants).  



PBDEs didn't come into use until the 1960's and 1970s. (245b)  They are essentially used as fire retardants in consumer plastics, especially electronic devices such as TVs and computers.  According to a Japanese study, "Several toxic effects on the thyroid system or on neurodevelopment have been reported in experimental animals exposed to PBDEs." (90)  Note in Section 1.2.b.1 at this link that increases or decreases in thyroid levels have been reported to "cause irreversible neurological damage" during development of the brain.  Also note in Section 1.7.1 at this link  about endocrine-disrupting, anti-androgenic, testosterone-reducing effects of PBDEs, which could well be already at toxic levels according to the EPA, even while levels in humans are rapidly increasing.  And remember from earlier that a breastfeeding American infant receives a dosage of PBDEs from mother's milk alone that is about 20 times as high as the total average adult intake.  Remember also that current exposure to PBDEs alone is likely sometimes to be at toxic levels, not to mention the other toxins that are also known to be present in breast milk


Diesel emissions:

Remember that the dioxin component of diesel emissions in the U.S. approximately doubled in the last 13-year period for which the EPA provides data.(96)   (Bear in mind from earlier that dioxins in breast milk are known to especially greatly exceed the safe level estimated by the EPA.  Considering that dioxins from diesel emission have been rising greatly, it should be safe to assume that diesel emissions in general have also been increasing substantially.  Note that diesel engine exhaust was classified as a known human carcinogen by the EPA in 2012.   One of the other toxic components known to be contained in the rising diesel emissions, PAHs (known to cause cancer in animals), has almost certainly also continued to increase in atmosphere inhaled by many nursing mothers and mothers-to-be.  Note in the next paragraph how closely PAH concentrations in breast milk are related to exposure to diesel exhaust.

The chart on the left (from a Japanese study) indicates high concentrations of 
five different kinds of PAHs in breast milk of rats that had been exposed to 
diesel exhaust (DE) for six hours a day from the seventh day of gestation until 
14 days after birth, with concentrations similar to those in downtown 
Kanazawa, Japan37b  (Kanazawa is the study's lead author's university city, 
population 450,000).  PAH concentrations in the breast milk of the exposed 
rats ("DE") were two to three times higher than in the control group, despite 
the fact that the exposure was apparently only moderately high; note that this 
exposure of 
the rats to diesel exhaust, for only six hours a day, was not an especially high 
dosage.  As indicated in this chart, lactation appears to be an efficient means 
of taking in toxins from the atmosphere and concentrating them in breast milk.  
Although information about PAHs in cow's milk does not appear to be available 
for comparison, it is probably safe to assume that a much higher percentage of human 
mothers and mothers-to-be than of cows has a close exposure to diesel exhaust, from 
vehicular traffic, railroads, ships, port and canal dredging machinery, construction equipment, etc.   


An Italian study found PAHs to be higher in lactating women who smoke.  The specific form of PAH that was investigated in this study was benzo(a)pyrene (BaP), which is classified as a Class 1 carcinogen by the International Agency for Research on Cancer.  There is no determination of a maximum tolerable amount in breast milk, so the Acceptable Daily Intake (ADI) for drinking water was used in the study. "For babies whose mothers belonged to the non-smoker rural category, daily BaP equivalent intake during a six-month nursing period was below the ADI."  But intake of BaP in breast milk by infants of urban smokers showed values "from about seven times, up to 1000 times higher than ADI." (emphasis added)  Breast milk of urban non-smokers was intermediate in concentrations.(26a)   Note that BaP is also a major component of diesel exhaust,(90c) as well as of tobacco smoke.


Authorities writing about dioxins, which are better known than PAHs, emphasize the predominant role of diet as being the major source of those toxins into the body (and thereby into breast milk).  It is worth taking special note of the fact that, in the cases of the also-toxic PAHs from diesel exhaust and tobacco smoke (as indicated above) and also PBDEs from electronics, the inhalation route is also an important means of absorbing environmental toxins which can then become concentrated in breast milk.  In that regard, remember from earlier that PAHs are not only carcinogens but also endocrine disruptors, capable of damaging neurological development.  Then note that a study of effects of proximity to California freeways (published in 2011) found a doubled percentage of autism among infants residing within about 1000 feet of freeways, compared with those farther away. (194)


The above two studies appear to be the only ones published regarding presence in breast milk of PAHs (including BaP).  They show carcinogens and probable developmental toxins being found especially concentrated in breast milk following rather ordinary exposures of the mothers to diesel emissions and tobacco smoke.  The amount of PAHs in the breast milk was directly related to the extent of the mothers' exposures to the chemicals. The finding of carcinogenic intake of BaP by breastfeeding being up to 1000 times the acceptable level for infants of urban smoking mothers, while levels were in the safe range for rural non-smokers, highlights how extremely effective lactation is at taking in environmental pollutants in typical amounts and concentrating them in breast milk. 


Mothers should not necessarily feel safe about their breast milk if they are rural non-smokers.  Whereas PAH's are apparently mainly taken in by inhalation, dioxins are mainly taken in by way of food; unless one lives in an unusually low-pollution food-source region, the only way to avoid typical concentrations of dioxins in breast milk is to adopt a basically vegetarian diet many years before breastfeeding starts.  Also, residential wood-burning emissions are a major source of BaP(26b)  and particulate matter, and a significant source of lead, typically emitted in the immediate air supply of both lactating mothers and infants. Breast milk in rural Italian mothers was probably uniformly within acceptable limits of BaP at least partly because there is relatively little residential wood burning in sunny Italy, with minimal forests.  It is also important to bear in mind that backyard burning, often done in rural areas, has become the largest single source of releases of dioxins to the atmosphere in recent years, according to the EPA.  In addition, high levels of PBDEs in breast milk apparently result mainly from exposure of mothers to air around electronic devices. (See earlier in this section.)

One can be safe in assuming that most cows do not have nearly the exposure to diesel emissions, tobacco smoke, air surrounding electronic devices, and residential wood-burning pollution that human mothers have, not to mention not eating meat, fish and dairy products into which toxins have bio-accumulated.   


Continuing increases of developmental toxins in environments of developed countries:

The EPA reports that major smokestack sources of dioxins in the atmosphere have declined greatly in recent decades as a result of regulatory efforts, but dioxins are extremely persistent in the environment, especially in soil; and releases of dioxins in diesel emissions (which often reach heavily at ground level into highly-populated areas) have continued to increase rapidly, as of the most recent EPA data (for year 2000).  It is probable that diesel emission pollution will continue to increase in the U.S., as more and more decades-old diesel-powered vehicles continue in operation in the U.S. without emission restrictions, unlike in many or most European countries.   Note that, in addition to typically consisting partly of dioxins, diesel emissions as a whole are known separately to be endocrine disruptors and carcinogens.  Backyard burning (including its typical major component of plastics trash, which contributes to formation of dioxins) is difficult to control and became the largest single source of dioxin releases in the U.S. environment as of the latest EPA inventory (for year 2000) above source, (34) Table 1-4).  The worst effects of the pollution generated would be on infants and child-bearing women living in the areas near where the burning is done, but the dioxins released would also enter the food chain of the general population (this burning is mostly done in rural areas).  The emissions released would also be deposited on soil, water supplies, and in the form of dust, to which all infants downwind could be exposed.


Regarding the rapidly-increasing dioxins from diesel emissions, typically reaching closely into populated areas, those emissions are probably what basically underlie the doubled risk of autism found among infants residing within about 1000 feet of freeways in a California study.(194)  (Diesel emissions are known to be many times higher than unleaded gasoline emissions in dioxin content.)(198)


BPA (Bisphenol A) is another recognized endocrine disruptor, to which people including future mothers and nursing mothers are especially exposed via its use in plastic packaging of food and drinks, including in linings of metal cans. Production of BPA in the U.S. increased over 100-fold between 1991 and 2004.  The National Toxicology Program (NTP) has “some concern” for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to BPA.  The U.S. Geological Survey is confident that adult exposure to BPA affects the male reproductive tract, and that long-lasting effects in response to developmental exposure to BPA occur in the brain, male reproductive system, and metabolic processes.(38)

 A review of studies of exposure of pregnant and lactating mice to a "low, environmentally relevant dose of BPA" found that this had observable effects in the offspring of behavioral responses to novelty, of exploration behavior and activity in various environments, and of sensitivity to rewards.(38a) 


PBDEs have also been increasing extremely rapidly in environments of developed countries.  (See Section 1.7.1 at this link )



More on how these toxins harm development:

In addition to possible or known endocrine-disruption and sometimes potent mutagenic properties of PAHs,(39) many of the derivatives, also, "have been found to be highly mutagenic." (same EPA source, p. 2-90)  Mutagens should be of special concern because they can affect the descendants of a person who outwardly appears to be unaffected. Elsewhere in this paper there are various references to possible effects of environmental toxins on pregnant women and developing infants, and for brevity the possible effects on the genetic material in future parents of both genders will not be mentioned at the same time.  But it should be kept in mind that mutagens could be affecting genes of both men and women now in ways that may not be apparent in them but which could be expressed in their future children.


A number of studies indicate that dioxins and dioxin-like compounds (which include some types of PCBs) decrease circulating thyroid hormone levels, which can impair the brain development of offspring.  According to the EPA's web page on health effects of PCBs, "newborn monkeys exposed to PCBs showed persistent and significant deficits in neurological development, including visual recognition, short-term memory and learning. Some of these studies were conducted using the types of PCBs most commonly found in human breast milk."  "Even low levels of dioxin or PCB exposure during the perinatal period can greatly influence neurological development" in this way and "can cause irreversible neurological damage.(40)  Most major sources of releases of PCBs to the environment were discontinued in 1979, which helps explain the major decline in mental impairment among girls born in recent decades.  (Mental impairment of boys resulting from PCBs would have declined also, but that was obscured by increase in mental impairment of boys resulting from something new that predominantly affects boys, such as autism; as PCBs in the environment declined, other neuro-developmental toxins that are known to specifically affect males were increasing, such as dioxins from diesel emissions, other diesel emission components, and the especially rapidly increasing PBDEs.)   Countering the drop in PCB releases from industrial sources, PCBs are also part of diesel emissions,(40a) which have been increasing rapidly in the U.S., according to the EPA's latest data.   PCBs are also extremely persistent in the environment and (along with other variations of dioxins and dioxin-like chemicals) are still very significant in harmfulness.   As of 2006, the EPA reported that "one-third of general population TEQDFP (dioxin toxic equivalency) exposure is due to PCBs." (41)    

To illustrate the potency of some of these developmental toxins, it is worth considering a test performed on rhesus monkeys with Aroclor 1248, a commonly-used commercial product that contained PCBs.  According to the U.S. ATSDR, Aroclors were “useful in a wide variety of applications, including dielectric fluids in transformers and capacitors, heat transfer fluids, and lubricants…. PCBs are combustible liquids, and the products of combustion may be more hazardous than the material itself.” (43)  Other common uses of PCBs included fluorescent light ballasts and plasticizers.(44)    “In rhesus monkey infants whose mothers were or had been exposed to Aroclor 1248 during gestation and lactation, behavioral testing showed hyperactivity and retarded learning ability….  These effects were reported at doses of about 0.006 mg Aroclor 1248/kg bw/day to the mothers.” (45)  Assuming a recognized average weight of 5.3 kg (12 pounds) per female monkey, this works out to 0.032 mg per monkey per day, or a dose of less than one 800,000th of one ounce of Aroclor per day per gestating/lactating female monkey.   When considering the effects of 1/800,000th of an ounce of a PCB-containing product, also bear in mind that 600,000 tons of PCBs were produced in the U.S. between 1930 and 1977, that they are very stable and are contained in considerable equipment that is still in use (and sometimes leaking); they are also heavily present in landfills, which are a major source of emissions of toxins to the atmosphere (especially during fires), not to mention the landfills’ drainage to water supplies.  Although PCBs are no longer produced in the U.S. and have recently been banned in most countries, their continued presence in imported products is open to question.  Also, indoor air in houses with floors finished with PCB-containing wood finish have been found to contain high levels of PCB. (46)  At the rate of wide use of a chemical for a half century or more before determining that it is too toxic (as was the case with the pesticides endosulfan and dicofol), one may reasonably wonder about the safety of the materials that are now being used in place of PCBs.  (Yes, most of the thousands of chemicals introduced into use in recent decades have not been tested for safety.)




  Pesticides also, including some that are used residentially, have been widely found in breast milk.(92).  Section 1.6.a at provides details about connections between various pesticides to which fetuses and infants are exposed and (a) autism, (b) other changes in social behavior and brain development, (c) attention deficit disorders and hyperactivity disorders, (d) feminization of males and (e) masculinization of females.

Bromine is another neurological toxin excreted in breast milk; bear in mind that a mother could absorb bromine through her skin while in a pool or spa treated with bromine as a disinfectant.

Most of the research that has found developmental harm to result from exposure to these chemicals was based on tests with animals, but “the chemical structures of hormones and their receptors are very similar among vertebrates, including humans. A chemical that binds with an estrogen receptor in mice is almost certainly going to bind with an estrogen receptor in people.” (93)   Research with human data has verified the results from animal tests regarding the testosterone-reducing, de-masculinizing effects of phthalates, another toxin known to be present in breast milk. (Section 1.6.b at

Some commentators downplay the significance of the extraordinarily high dosage of toxins received by infants in breast milk, pointing out that, if one looks at that dosage spread out over a typical 70-year lifespan, it becomes a relatively minor addition to the typical total lifetime exposure to the toxins.  The problem with that viewpoint is that permanent, life-impairing neurological damage as well as childhood cancer can occur during infancy while effective exposure levels are many times higher than the later lifetime average, early levels that are especially high in relation to the infant's vulnerable stage of development.

As explained above, breast milk today is not the beneficial, safe substance today that it was in earlier times:  Essentially all of the above toxins have begun to become major problems in the environment only beginning in the mid-20th-Century, with some of them (such as PBDEs, BPA and some pesticides) not becoming significant until very late in the 20th Century.  Many new types of pesticides were introduced only in the 1980's..(92). 


Message to health professionals, scientists, and others reading this paper:  This author cordially invites you to indicate your reactions to the contents presented here.  As of now, new parents almost never hear anything but completely one-sided promotion of breastfeeding, with no mention of possible drawbacks except in cases of serious problems on the part of the mother.  If you feel that parents should be informed about both sides of this question and thereby enabled to make an educated decision in this important matter, please write to the author of this paper.  Also, if you find anything here that you feel isn't accurately drawn from trustworthy sources or based on sound reasoning, please by all means send your comments, to  All comments will be posted at the end of this paper, at ***

To return to the main page of this website, click on the "back" arrow on your browser or click on .



(28) ATSDR  web page "Public Health Statement for DDT, DDE, and DDD,"September 2002, Section  at

The exact wording that was paraphrased here was, "The proper development of many systems and functions depends on the timely action of hormones, particularly sex steroids; therefore, interfering with such actions can lead to a wide array of effects that may include altered metabolic, sexual, immune, and neurobehavioral functions. Effects of this type, that occur following exposure during fetal life via the placenta or early in life caused by either direct exposure to chemicals or exposure via maternal milk, are discussed in this section."  



(30) From

(31) Committee on Developmental Toxicology, Board on Environmental Studies and Toxicology, in  Scientific Frontiers in Developmental Toxicology and Risk Assessment (2000) , Commission on Life Sciences,  The National Academies Press, p. 56

(32) United States Office of Research May 25, 2001 Update, Environmental Protection and Development Agency, Dioxin: Scientific Highlights from Draft Reassessment (2000)

(33) Male Reproductive Health and Environmental Xenoestrogens Jorma Toppari,et al. Environmental Health Perspectives - Vol 104, Supplement 4 - August 1996

(33a)  Lower Serum Testosterone Associated with Elevated Polychlorinated Biphenyl Concentrations in Native American Men

Alexey Goncharov, et al., Environ Health Perspect. 2009 September; 117(9): 1454–1460. Published online 2009 May 20. doi: 10.1289/ehp.0800134 PMCID: PMC2737025  at

(34) ATDSR document on dioxins, section on environmental sources

(34a)  National Academies of Science report on dioxins in the food supply.

(34b) in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day."   In the EPA’s “Glossary of Health Effects”, RfD is defined:  “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”

(34c)  U.S. EPA. Estimating Exposure To Dioxin-Like Compounds - Volume I: U.S. Environmental Protection Agency, Washington, D.C., EPA/600/8-88/005Ca., 2002, revised 2005 –,  Section II.6, "Highly Exposed Populations" (nursing infants are considered to be one of the highly-exposed populations), 4/94 (p. 39)  "Using these procedures and assuming that an infant breast feeds for one year, has an average weight during this period of 10 kg, ingests 0.8 kg/d of breast milk and that the dioxin concentration in milk fat is 20 ppt of TEQ, the average daily dose to the infant over this period is predicted to be about 60 pg of TEQ/kg-d."

(34d) Schecter, A., et al. Chlorinated Dioxins and Dibenzofurans in Human Tissue from General Populations: A Selective Review, Environmental Health Perspectives Supplements 1994; 102(Supple 1): p. 159-171  and  Schecter, A., et al. Congener-specific Levels of Dioxins and Dibenzofurans in U.S. Food and Estimated Daily Toxic Eequivalent Intake, Environmental Health Perspectives Journal 1994; 102(11): p. 962-966.

(34e)  Chemosphere.

 2007 Jan;66(2):311-9. Epub 2006 Jun 14.  A comparison of PCDD/PCDFs exposure in infants via formula milk or breast milk feeding.   Hsu JF, et al.

(35) "Technical Information for California Health Officials,"  May 2003, California Department of Health Services, Environmental Health Investigations Branch, p. 6

(36) Executive Summary:  Assessment of the health risk of dioxins: re-evaluation of the Tolerable Daily Intake (TDI)   WHO Consultation  May 25-29 1998, Geneva, Switzerland, p. 27

(37) PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants, Jiyeon Yang et al. Chemosphere 46 (2002) 419–428

(37a)  Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber1 and Phillips2  VOLUME 110 | NUMBER 6 | June 2002 • Environmental Health Perspectives

(37b)  Transfer of Polycyclic Aromatic Hydrocarbons to Fetuses and Breast Milk of Rats Exposed to Diesel Exhaust, Tozuka, Watanabe et al., Kanazawa University and Tokyo Metropolitan Public Health Research Institute; Journal of Health Science 50(5) 2004 pp. 497-502


(38) ToxTown of National Library of Medicine, at

(38a) Effects of developmental exposure to bisphenol A on brain and behavior in mice. Palanza P, et al., Environ Res. 2008 Oct;108(2):150-7. At

(39) EPA/600/8-90/057F  May 2002, Health Assessment Document for Diesel Engine Exhaust, Table 2-22.  National Center for Environmental Assessment, Office of Research and Development, EPA

(40) Industrial Health 2000, 38, 259–268 Review Article:  The Effects of Dioxin on Reproduction and Development  Junzo YONEMOTO  National Institute for Environmental Studies, Japan  p. 262;  Glorieux et al., 1988; Rovet et al., 1987; Haddow et al., 1999)." (Prioritization of Toxic Air Contaminants  -- Children's Environmental Health Protection Act (State of California), October, 2001

(40a)  C.A. Laroo et al., Emissions of PCDD/Fs, PCBs and PAHs from a Modern Diesel Engine Equipped with Catalyzed Emission Control Systerms, Environmental Science and technology, ACS Publications, June 30, 2011

(41) EPA/600/P-03/002F, November 2006: p. 11-28

(42) Reijnders, P.J. (1986) Reproductive failure in common seals feeding on fish from polluted coastal waters. Nature, 324, 456–457.

(43) from the  ATSDR website page on Aroclors


(45) Ahlborg UG, Hanberg A, Kenne K. Risk Assessment of Polychlorinated Biphenyls (PCBs). Environmental Report in the Nord Series. Nord 26. Copenhagen: Nordic Council of Ministers, 1992.

(46) Environ Health. 2008; 7: 2. Published online 2008 January 17. doi: 10.1186/1476-069X-7-2  Rudel et al; licensee BioMed Central Ltd.  PCB-containing wood floor finish is a likely source of elevated PCBs in residents' blood, household air and dust: a case study of exposure


(81b)  Concentration of Persistent Organochlorine Compounds in the Placenta and Milk of the Same Women, Katarzyna Czaja et al., Ch. 21 of Persistent, Bioaccumulative, and Toxic Chemicals I, Robert L. Lipnick et al. editors, ACS Symposium Series, American Chemical Society, 2001; citing Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991.  Findings of above confirmed in animal tests, with even greater contrasts, in Ahlborg et al., Risk Assessment of Polychlorinated Biphenyls (PCBs), Nordic Council of Ministers, Copenhagen.  Report NORD 1992; 26

(81c) U.S. EPA  (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at

(81d) Table 5-4 of above source

(81e)  Section 5.6.2 of above source

(81f)  Section 4.7 of above

(81g)  Section 5.6.2 of above.  The EPA states the figure as "44.1 ng/g lwt"  (44.1 ng = 44,100 pg).  For comparison purposes, the lipid (fat) weight indicated here needs to be converted to whole weight, which can be done as follows:  The EPA here assumes a fat content of 4%.  Using that figure, 44,100 pg/g lwt becomes 1760 pg/g wwt.

(81h)  Section 4.1 of ATDSR document on PBDEs at


(81j)  Giroux, D., G. Lapointe, and M. Baril. Toxicological Index and the Presence in the Workplace of Chemical Hazards for Workers who Breast-feed Infants, American Industrial Hygiene Association Journal 1992; 53(7):


(81l) National Institute for Occupational Safety and Health. Criteria for a Recommended Standard: Occupational Exposure to Ketones. DHEW (NIOSH) Publication No. 78-173, 1978,  quoted in

(81m) Axelson, O., et. al., Current Aspects of Solvent Related Disorders. In Developments in Occupational Medicine (ed Carl Zenz), Yearbook Medical Publishers Inc., Chicago, pp. 237-59, 1977, quoted in

(81m1)  Reproductive Toxicology and Occupational Exposure, J. Messite, MD, and M.B. Bond, MD, in Developments in Occupational Medicine, Carl Zenz, MD, Sc.D, ed., 1980

(81n) Lactational Transfer of Volatile Chemicals in Breast Milk, Jeffrey Fisher et al., American Industrial Hygiene Association Journal, June, 1997, p. 429.


(81p)  "International Chemical Safety Card". National Institute for Occupational Safety and Health. Retrieved 2 February 2006.

(81r)  Black, RE; Hurley, FJ; Havery, DC (2001). "Occurrence of 1,4-dioxane in cosmetic raw materials and finished cosmetic products". Journal of AOAC International 84 (3): 666–70. PMID 11417628.


(81t)  EXPLORATION OF PERINATAL PHARMACOKINETIC ISSUES  Contract No. 68-C-99-238, Task Order No. 13  Prepared for:  Office of Research and Development,  U.S. Environmental Protection Agency  Prepared by:  Versar, Inc.  EPA/630/R-01/004   Section,  at

       (81u) Oxford Journals  Medicine Brain  Volume 129, Issue 2  Pp. 290-292.   Brain (February 2006) 129 (2): 290-292. doi: 10.1093/brain/awh729 Cognition, emotion and the cerebellum  Jeremy D. Schmahmann et al.

       (81v)  Exploration Of Perinatal Pharmacokinetic Issues (Final Report),  Contract No. 68-C-99-238  Task Order No. 13,  Prepared for: U.S. Environmental Protection Agency, by:  Versar, Inc., Springfield, VA,  Section

And   Lok, E. 1983. The effect of weaning on blood, hair, fecal and urinary mercury after chronic ingestion of methylmercuric chloride by infant monkeys.  Toxicology Letters, Volume 15, Issues 2–3, February 1983, Pages 147–152,  abstract at

       (81w)  Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, Roberts et al., published June, 2013 in Environmental Health Perspectives, at

(81x) Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at

(81y)  quoted from EPA web page at

(82) National Academies Press: Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment (2006), Board on Environmental Studies and Toxicology, National Academy of Sciences; the original source is not quoted directly because it is part of a draft, not for quoting

(82a) ATSDR    Public Health Statement for Polychlorinated Biphenyls (PCBs),  November 2000, Balfanz et al. 1993; MacLeod 1981; Wallace et al. 1996,  p. 569

(82b)  Pediatric Research (2001) 50, 331–336; doi:10.1203/00006450-200109000-00007  Early Childhood Determinants of Organochlorine Concentrations in School-Aged Children, Wilfried Karmaus et al.

(82c)  Kommission “Human-Biomonitoring” des Umweltbundesamtes:  Stoffmonographie PCB - Referenzwerte für Blut   (Commission on Human Bio-Monitoring of the (German) Federal Environmental Office:  Substance Monograph on PCB - - Reference Values for Blood)  At , Section 8.3. found within , website of Umwelt Bundes Amt (German Federal Environmental Office).  This article cited for this breastfed infant exposure data the source:  Institut für Wasser-,Boden und Lufthygiene des Umweltbundesamtes, Kommission „Human-Biomonitoring“ des Umweltbundesamtes • Berlin:   Referenzwerte für HCB,b-HCH, DDT und PCB in Frauenmilch   (Institute for Water-, Soil and Air Hygiene of the Federal Environmental Office, Commission on Human Bio-Monitoring:  "Reference Values for HCB,b-HCH, DDT und PCB in Human Milk."  The text drawn on says, " "Die derzeit durchschnittlich vom Erwachsenen täglich aufgenommene Menge an PCB (ca. 0,02 μg PCB/kg KG [13]) liegt deutlich unter der ATD von 1 μg PCB/kg KG. Der gestillte Säugling erhält dagegen eine deutlich höhere PCB-Zufuhr (3 μg PCB/kg KG.", which Bing Translator translates as " "The amount taken daily average currently by the adults of PCB (approx. 0.02 μg PCB/kg bw [13]) is well below the ATD of 1 μg PCB/kg. The breastfed infant, however, receives a significantly higher PCB intake (3 μg PCB/kg bw."

(83) Infant Exposure to Dioxin-like Compounds in Breast Milk,  Lorber and Phillips  Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives   Also EPA Home/Research/Environmental Assessment: An Evaluation of Infant Exposure to Dioxin-Like Compounds in Breast Milk, Matthew Lorber (National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency) et al.

 (84) In Prioritization of Toxic Air Contaminants - Children’s Environmental Health Protection Act, October, 2001:  Dioxins

(85) Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants. Abraham K, Knoll A, Ende M, Päpke O, Helge H.  Children's Hospital, Virchow-Klinikum, Humboldt-Universität Berlin, Germany

(86) Regulatory Toxicology and Pharmacology, 37 (2003) 202 217 Dioxin risks in perspective: past, present, and future  Hays and  Aylward  at

(87) Challenged Conceptions:  Environmental Chemicals And Fertility" 2005,  a publication of Stanford University School of Medicine, p. 4


(89) "Paying a Price for Loving Red Meat" in Personal Health, by Jane E Brody, New York Times: April 27, 2009


(89b)  Brominated Flame Retardants, Third annual report to the Maine Legislature, Jan. 2007, Maine Dept. of Environmental Protection, Maine Center for Disease Control and Prevention, Dr. Deborah Rice et al.

(90) Shokuhin Eiseigaku Zasshi. 2004 Aug;45(4):175-83. PubMed – NCBI   Polybrominated diphenyl ether flame retardants in foodstuffs and human milk. Akutsu K, Hori S.  Osaka Prefectural Institute of Public Health: 1-3-69, Nakamichi,Osaka 537-0025, Japan

(90a)  Zanieri L, Galvan P, Checchini L, Cincinelli A, Lepri L, Donzelli GP, et al. Polycyclic aromatic hydrocarbons (PAHs) in human milk from Italian women: influence of cigarette smoking and residential area. Chemosphere. 2007;67:1265–74., cited at

(90a1)  Quotation to be found at

(90a2)  The wonder of breasts Florence Williams  The Guardian, Friday 15 June 2012 

(90b) Particle and Fibre Toxicology, Effects of prenatal exposure to diesel exhaust particles on postnatal development, behavior, genotoxicity and inflammation in mice. Karin S Hougaard et al., National Research Centre of the Working Environment, Copenhagen, Denmark.  Published: 11 March 2008  Particle and Fibre Toxicology 2008, 5:3 doi:10.1186/1743-8977-5-3  This article is available from:


(91) CAS No: 7726-95-6)  Health-based Reassessment of Administrative Occupational Exposure Limits,  Committee on Updating of Occupational Exposure Limits, a committee of the Health Council of the Netherlands

(92) Environmental Health Perspectives, Vol. 109, No.1, Jan. 2001

(93) Challenged Conceptions: Environmental Chemicals And Fertility" 2005, a publication of Stanford University School of Medicine, p. 10

(96) An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000", EPA/600/P-03/002F, November 2006: especially Table 1-17.  2000 appears to be the most recent year for which the EPA provides national dioxin release data

(194)   "Residential Proximity to Freeways and Autism in the CHARGE Study" , Environmental Health Perspectives, Published in 119(6) Jun 2011, Heather E. Volk, Irva Hertz-Picciotto et al., reported (with doubling comment) in ScienceDaily (Dec. 17, 2010), "Proximity to Freeway Associated With Autism"

(198) Figure 1-8 in EPA/600/P-03/002F November 2006 An Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States for the Years 1987, 1995, and 2000

(244) TOXICOLOGICAL PROFILE FOR LEAD, ATSDR  August 2007, Section 3.3.2

(245) ATSDR Section 3, p. 264

(245b)   U.S. EPA  (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at  Executive Summary, p. xxiii

(254) EPA-452/R-97-006, December 1997, Table 2-3